Guias de manejo melanoma no operable 2026

A clinical practice guideline has been published that provides recommendations on the use of systemic therapy in patients with unresectable, metastatic cutaneous melanomas. These guidelines were published by Cancer Care Ontario.

The evidence-based recommendations apply to adults with unresectable nodal or distant metastatic cutaneous melanoma, defined as American Joint Committee on Cancer (AJCC) 8th edition stage IIIC/D or stage IV, who are candidates for systemic therapy. Intended users of the guideline include medical oncologists, dermatologists, and other clinicians involved in melanoma care. The recommendations reflect a decade-long therapeutic shift driven by immune checkpoint inhibitors — including anti-programmed cell death protein 1 (anti-PD-1) inhibitors, anti-cytotoxic T-lymphocyte-associated protein 4 (anti-CTLA-4) inhibitors, and anti-lymphocyte-activation gene 3 (anti-LAG-3) agents — and BRAF/MEK-targeted therapies.

First-Line Therapy: BRAF Wild-Type Disease

For patients with BRAF wild-type melanoma, recommended first-line options include nivolumab plus ipilimumab, nivolumab plus relatlimab, nivolumab monotherapy, and pembrolizumab monotherapy.

Nivolumab 1 mg/kg plus ipilimumab 3 mg/kg is to be administered intravenously once every 3 weeks for 4 total doses, followed by nivolumab 3 mg/kg every 4 weeks until progression, toxicity, or the need for other treatment considerations. Nivolumab 480 mg plus relatlimab 160 mg should be administered intravenously every 4 weeks until progression. Nivolumab monotherapy is to be administered intravenously in a dose of 3 mg/kg every 2 weeks or 6 mg/kg every 4 weeks, with either dose continued until progression, toxicity, or other considerations. Similarly, pembrolizumab is to be administered intravenously in a dose of 2 mg/kg every 3 weeks or 6 mg/kg every 4 weeks for a maximum of 2 years, with the potential for retreatment for 1 year.

Due to the evolving environment surrounding systematic therapy for unresectable, metastatic melanoma, indications and approvals are changing rapidly.

Evidence is anchored in a 2018 Cochrane review and multiple randomized controlled trials. Anti-PD-1 therapy (nivolumab or pembrolizumab) significantly improved overall survival (OS) and progression-free survival (PFS) compared with ipilimumab, with lower rates of grade 3-4 toxicity. Better PFS but higher rates of grade 3-4 treatment-related adverse events occurred with nivolumab combination therapy vs nivolumab monotherapy. Nivolumab plus relatlimab demonstrated improved PFS compared with nivolumab alone, with higher toxicity rates than nivolumab alone but lower than with nivolumab plus ipilimumab. While chemotherapy remains an option, immunotherapy is preferred due to superior survival outcomes.

First-Line Therapy: BRAF-Mutated Disease

For patients with BRAF-mutated melanoma, both immunotherapy and targeted therapy are recommended. In addition to the recommended treatment options for BRAF-wild type melanoma, patients with BRAF-mutated melanoma may also receive BRAF/MEK inhibitor combinations of dabrafenib plus trametinib, encorafenib plus binimetinib, or vemurafenib plus cobimetinib. However, immunotherapy is preferred as first-line treatment based on sequencing data.

Dosing for nivolumab plus relatlimab and nivolumab monotherapy are the same for patients with BRAF-mutated disease as patients with BRAF-wild type disease. Nivolumab plus ipilimumab is to be administered intravenously every 3 weeks for up to 4 doses, followed by nivolumab 6 mg/kg every 4 weeks until progression, toxicity, or other considerations. Pembrolizumab monotherapy is available intravenously for up to 2 years with a 1-year potential retreatment period in a dose of 2 mg/kg every 3 weeks, 4 mg/kg every 6 weeks, or 6 mg/kg every 4 weeks. Dabrafenib 150 mg should be taken twice daily and trametinib 2 mg should be taken once daily, both orally. Similarly, encorafenib 450 mg should be taken once daily while binimetinib 45 mg should be taken twice daily, both orally. Vemurafenib 960 mg should be taken twice daily with cobimetinib 60 mg once daily for 21 days with a 7-day rest period in each 28-day cycle.

Combination BRAF/MEK inhibitors vs BRAF monotherapy consistently demonstrated improved outcomes with a reduced mortality risk without increased toxicity in pooled analyses. Improved PFS and OS were observed with encorafenib plus binimetinib vs vemurafenib. Other trials similarly supported dabrafenib plus trametinib.

Triplet regimens (BRAF/MEK plus anti-PD-1/PD-L1) yielded mixed results. Some analyses demonstrated PFS improvements but triple-therapy regimens did not consistently improve OS and were associated with higher grade 3-4 toxicity than double-therapy regimens.

Sequencing trials provide key guidance. Superior 2-year OS and PFS were observed when patients received nivolumab plus ipilimumab first, followed by targeted therapy at progression. Sustained superiority of immunotherapy-first strategies was confirmed at 5 years. Initial immunotherapy, with or without short targeted therapy, was preferred over targeted therapy-first approaches. Continuous BRAF/MEK dosing was superior to intermittent dosing.

PD-1-Refractory Disease

For patients with BRAF wild-type melanoma who are refractory to PD-1 monotherapy (including both primary and acquired resistance), recommended options include nivolumab plus ipilimumab or pembrolizumab plus ipilimumab. Nivolumab plus ipilimumab improved PFS compared with ipilimumab alone.

For PD-1-refractory BRAF-mutant melanoma, options include combination immunotherapy with nivolumab plus ipilimumab, nivolumab plus relatlimab, or pembrolizumab plus ipilimumab, as well as BRAF/MEK inhibitors. Subgroup analyses showed PFS benefits for pembrolizumab in certain previously treated BRAF-mutant populations.

Dosing schedules for all regimens are consistent among patients who are and are not refractory to PD-1 monotherapy.

Molecular and Clinical Subtypes

For NRAS-mutant melanoma, binimetinib may be considered with or without immunotherapy. Binimetinib improved PFS compared with dacarbazine, although responses were modest.

For KIT-mutant melanoma, evidence is limited to single-arm studies. Due to low-quality evidence and absence of randomized controlled trials, no specific recommendation is made beyond following general systemic therapy guidance.

For brain metastases, nivolumab plus ipilimumab is recommended. In trials evaluating patients with asymptomatic brain metastases, greater rates of intracranial response were observed with combination therapy vs nivolumab alone. Combination immunotherapy was also favored over chemotherapy-based approaches based on 7-year OS data. Further, BRAF/MEK inhibitors demonstrated promising intracranial response rates in BRAF V600-mutant brain metastases, although responses were less durable than in extracranial disease. Radiation therapy, particularly stereotactic approaches, remains an important component of multidisciplinary care.

Implementation and Evidence Limitations

For all patients, clinical trial participation is encouraged when standard options fail or are not acceptable.

The guideline emphasizes shared decision-making, balancing OS/PFS benefits against toxicity, patient comorbidities, and preferences. Toxicity profiles vary significantly, particularly with combination immunotherapy.

Key limitations include the lack of direct head-to-head randomized controlled trial comparisons between immunotherapy and targeted therapy, limited predictive biomarkers beyond BRAF mutation status, and reliance on subgroup analyses for brain metastases and refractory populations. Heterogeneity across trials precluded meta-analysis. Cost-effectiveness was outside the scope of these recommendations.

Future Directions

Further biomarker-driven research is needed to personalize therapy, optimize sequencing, and refine treatment duration strategies. Ongoing trials in NRAS-mutant disease and novel combinations may further evolve the therapeutic landscape.

Overall, the guideline reflects a paradigm in which immunotherapy, particularly in blocking combination immune checkpoints, provides durable survival benefit and is generally favored as first-line therapy, with targeted therapy integrated strategically based on mutation status, disease progression, and clinical circumstances.

Guideline authors concluded, “Due to the evolving environment surrounding systematic therapy for unresectable, metastatic melanoma, indications and approvals are changing rapidly.”

References:

Petrella T, Kellett S, Knight G, et al; Melanoma Disease Site Group. Systemic treatments for unresectable and metastatic cutaneous melanoma. Cancer Care Ontario. Published January 5, 2026. Accessed February 17, 2026. https://www.cancercareontario.ca/en/guidelines-advice/types-of-cancer/79966

Lisa Kuhns, PhD

Lisa Kuhns, PhD is an experienced medical writer specializing in news-focused content for healthcare professionals. With over 15 years in the life sciences and 5 years of freelance experience, she brings a keen editorial eye and scientific rigor to the development of timely, clinically relevant news articles and summaries. Lisa also has extensive experience supporting accredited continuing medical education (CME), including the development of needs assessments and expert-driven slide decks across multiple therapeutic areas. Her work supports evidence-based clinical decision-making and bridges science and medicine to keep clinicians informed and engaged. Website: www.lgkmedicalwriting.com LinkedIn: https://www.linkedin.com/in/lisakuhns/

Espectro de Lesiones de Spitz

Exploring Spitz nevi in the molecular era

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Dermatopathologists discuss how to approach spitzoid lesions and how molecular testing can aid in assessing their potential malignancy.

Feature

By Allison Evans, Assistant Managing Editor, April 1, 2026

Spitz nevi. Spitz tumor. Spitz melanoma. It has long been recognized that the histopathologic differential diagnosis between a Spitz nevus and melanoma — and the spectrum in between — can be challenging, with hazards related to under- and overtreatment. The advent of advanced molecular techniques like next generation sequencing (NGS), conventional or microarray comparative genomic hybridization (CGH), and fluorescence in situ hybridization (FISH), have provided new sophisticated tools to assist with this vexing differential diagnosis. 

Spitz nevus is named after Sophie Spitz, a pathologist who reported a case series of “melanomas of childhood” in 1948. Nearly all of Spitz’s original series of 13 cases are now regarded as representing Spitz nevi, with only one case having proved to be a melanoma resulting in metastasis and death. 

“This case series fundamentally changed our understanding of these lesions,” said Alina Bridges, DO, FAAD, director of cutaneous pathology at Northwell Health and director of dermatopathology at the Zucker School of Medicine at Hofstra/Northwell. 

Spitz refers to a family of melanocytic tumors that have commonalities, which include certain morphologic features under a microscope but also common genomic features, said Pedram Gerami, MD, FAAD, IDP Foundation professor of skin cancer research and professor of dermatology and dermatopathology, pathology, and pediatrics at Northwestern’s Feinberg School of Medicine.

“In 2013, the primary genomic drivers of Spitz were discovered,” he explained, “which allowed us to use genomics to more objectively and definitively determine if a lesion belongs to the Spitz family and to exclude mimickers of Spitz when the genomics do not match a Spitz profile.” 

To biopsy or not

According to Dr. Gerami, it is not necessary to biopsy all Spitz nevi. “However, prior to the biopsy, we don’t always know if we are dealing with a lesion in the Spitz family or a mimicker of Spitz. If the lesion is in the Spitz family we may not necessarily know if we are dealing with a Spitz nevus, atypical Spitz nevus, Spitz tumor (also called a melanocytoma), or Spitz melanoma.”

It’s a matter of risk management, he continued. “If you imagine the Spitz spectrum from Spitz nevus to atypical Spitz nevus to Spitz tumor to Spitz melanoma, in a prepubertal child the probability of being toward the benign end of this spectrum is significantly higher. In prepubertal children with symmetric macular lesions or even symmetric small papular lesions, observation is completely acceptable.” 

“Biopsies should be done any time the lesion exhibits atypical features such as a larger lesion — greater than 1 cm — exhibiting rapid growth or is ulcerating, if there’s any asymmetry, or if you have a patient who is older or post-pubertal,” Dr. Bridges said. 

In the ages between puberty and 40, the decision to biopsy is often made on a case-by-case basis, Dr. Gerami noted. “In a patient older than 40, the probability of malignancy in a lesion with a clinically spitzoid appearance becomes significant enough that I typically would biopsy these. The greatest threat is not a malignant Spitz melanoma but rather a conventional malignant melanoma mimicking a Spitz.”

“If the pigmented lesion in a child is a classic fit for a Spitz nevus, including the dermoscopy findings and the clinical evolution, then it can be safely monitored,” agreed Jeffrey North, MD, FAAD, professor of dermatology and pathology and managing director of UCSF Dermatopathology and Oral Pathology Service. 

“But it really needs to match all of those characteristics — symmetrical appearance, well circumscribed, no rapid growth, a uniform starburst pattern or globular pattern on dermoscopy.” He also noted the importance of ensuring the patient has the means to reliably follow up so the lesion can be monitored if a biopsy is not done.

Advances in dermatopathology

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Learn more about the latest trends and developments in dermpath.

Excision

According to the National Comprehensive Cancer Network (NCCN) Guidelines, the lesion should be removed in its entirety, Dr. Bridges said. “Dermatologists should do an excisional or complete biopsy, whether or not that’s a deep shave, a punch biopsy for smaller lesions, or an elliptical excision so that you can get around it with 1- to 3-millimeter margins.”

The ability to do molecular testing is mostly dependent on having adequate tumor DNA, Dr. Gerami agreed. “This can be compromised by doing small shaves of small lesions or small biopsies of large lesions, resulting in inadequate sampling. Regardless of the biopsy method, if the entire lesion is removed, this maximizes the likelihood that there will be enough tissue for immunostains and molecular testing.” 

“If I have just a small piece of tissue, then I have to sacrifice the number of immunostains that I’m going to do so that I have enough tissue left to do the molecular testing,” Dr. Bridges added.

This is particularly important when it comes to pediatric patients, she continued. “The parent and the child may not be too happy with you saying that you need to perform another excision to get a larger sample when we should have done it in the first place.”

Dr. North explained that he frequently sees Spitz tumors biopsied where they’re transected across the base, and oftentimes at the edges, and that really limits what the dermatopathologist can do in assessing the neoplasm. 

“We may be able to do molecular testing, but we can’t see if there’s good dermal maturation, if the lesion is well circumscribed — we can’t see what the bottom of the tumor looks like. Sometimes, a Spitz tumor may have an atypical part that’s not visible in the superficial part,” he added.

Diagnosing Spitz lesions: Case examples

Dr. Bridges highlighted one of her cases in which she received a specimen to rule out a dermatofibroma. “It may be challenging to clinically suspect Spitz nevi because they may not be pigmented. With immunostains and molecular testing, I rendered a diagnosis of Spitz melanoma as opposed to severely atypical Spitz nevus.”

“You can’t tell based solely on histomorphology, and I only did a few immunostains because I had very little tissue. I tried to see if there was any mitotic activity — there wasn’t. I sent this for a chromosomal microarray (similar to comparative genomic hybridization), which identified four copy number alterations; anything greater than three is considered suspicious for melanoma.”

In another of Dr. Bridge’s cases, a teenager presented with a history of a lesion on the ear. A superficial shave biopsy was performed, and it was diagnosed as a Spitz nevus. The lesion recurred and a deeper shave biopsy was performed. “The lesion was very atypical; it had three mitoses and was diagnosed as a Spitz melanoma based on the immunostains.”

“The first workup that was done came from haemotoxylin and eosin (H&E) and the second one came from immunostains. When I got the case, I did molecular testing and was able to downgrade the lesion to a severely atypical Spitz tumor rather than a Spitz melanoma,” she added.

Exploring Spitz: A spectrum of Spitz melanocytic lesions

Spitz nevi - Definitively benign

Atypical Spitz nevi - Definitively benign but with atypical histologic features

Spitz tumors - Borderline morphologic features but with most cases having an indolent clinical course

Spitz melanoma - Malignant melanoma version of a Spitz

Molecular diagnostics

Advances in molecular techniques have revealed many genetic differences between benign nevi and melanomas. Next generation sequencing, chromosomal microarray and/or CGH, and FISH are all tests that can be useful in certain scenarios to assess Spitz neoplasms and determine where they lie on the Spitz spectrum.

“Over the years that I’ve practiced, I have a lot more satisfaction handling these lesions,” Dr. Bridges said. “Before it was very ambiguous. You could say that it’s benign or atypical, but you couldn’t definitively rule out malignancy. We used to use the phrase ‘uncertain malignant potential’ all the time for these lesions, but now because of advanced immunostains and molecular testing, I can not only diagnose, but I’m almost prognosticating as well.”

The most important thing to determine is whether you are really dealing with a Spitz or a Spitz mimicker, Dr. Gerami emphasized. “Melanocytic tumors with mutations in BRAF, NRAS, GNAQ, and GNA11, for example, are immediately excluded from the Spitz family and belong to other classes of melanocytic neoplasia. However, an HRAS mutation or a characteristic Spitz fusion is highly consistent with classification in the Spitz family.” 

Immunostains

One of the most important stains is BRAF because all Spitz lesions will be negative for BRAF, Dr. Bridges said. “Conventional nevi usually have a single driver mutation — most commonly BRAF and less frequently NRAS.”

Dr. Bridges also uses the p16 stain to determine whether that tumor suppressor has been disabled. “In order to determine whether the specific mutation (CDKN 2A/2B genes) associated with melanoma is found, we need to do further molecular testing.”

While PRAME can be used, it has pitfalls because melanomas can be PRAME positive or negative, and benign lesions can be PRAME positive. Dr. Bridges recalled her aforementioned case of the teenager with the ear lesion that was downgraded from a Spitz melanoma to a severely atypical Spitz tumor. “She was diagnosed with Spitz melanoma because her p16 was lost and her PRAME was positive.”

Immunostains can be helpful, noted Dr. North. “Some can identify mutations that would exclude a Spitz family tumor. However, immunostaining to confirm a Spitz family tumor is limited. ALK staining to detect an ALK gene fusion in the Spitz family is the most reliable. The remaining immunostains for Spitz genetic drivers (e.g., NTRK1, ROS1, etc.) can be challenging to interpret and can lead to misdiagnosis. Most pathologists try immunostains before molecular testing.”

You can’t interpret any of these tests in isolation, Dr. Bridges remarked. “If there is severe atypia or if we’re in the category of Spitz tumors or melanocytomas and they have mitoses, then we’re going to be doing next generation sequencing to classify the lesion.” 

NGS and CGH

Comparative genomic hybridization can be helpful by providing the chromosomal copy number information and, in some cases, can show features suggestive of a Spitz gene fusion, but it’s not as comprehensive as NGS. “We rarely do CGH now because our next generation sequencing panel gives us the same data,” said Dr. North. “It provides mutation and fusion information about whether the tumor has a Spitz family genetic driver as well as potential additional progression mutations in other oncogenes and tumor suppressor genes. It also provides chromosomal copy number information similar to CGH to give a comprehensive genetic analysis of the tumor.”

Next generation sequencing identifies the specific driver alteration, so it definitively classifies the lesions, Dr. Bridges said. “Classification is important because even atypical Spitz tumors have an excellent long-term prognosis, despite having worrisome histologic or immunohistochemical features. There have been very large studies that showed event-free survival of 98% and overall survival of 100%.”

Spitz melanomas typically have additional pathogenic mutations, such as a TERT promoter mutation, and copy number aberrations, Dr. Bridges said.

NGS helps dermatopathologists classify the melanocytic pathway, Dr. North said. “This becomes really important because when you look at them under a microscope, they may look like a Spitz family tumor. But when you sequence them, they may not have the genetics of a Spitz tumor.”

“If there isn’t truly a Spitz genetic driver — if instead there is a BRAF mutation — that’s potentially a worse prognosis in an atypical tumor with spitzoid features. For the most part, even these very atypical Spitz tumors tend not to behave as aggressively. You can often only get this type of information with next generation sequencing,” he added.

PRAME sets its eyes on the road to fame

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Jason B. Lee, MD, FAAD, discusses preferentially expressed antigen in melanoma (PRAME) in evaluating melanocytic neoplasms.

FISH

There is a middle ground if there isn’t enough tissue, Dr. Bridges noted. “You could use FISH to detect chromosomal aberrations, which requires less tissue and has quicker turnaround time. However, 20% of melanomas will be FISH negative.” 

FISH is one of the oldest molecular tests used to assess Spitz tumors, said Dr. North. “Because it has the most studies published on it, it tends to be what’s most readily approved by insurance. With FISH you’re only able to look at four to eight segments of the genome, while NGS looks at a large amount of the genome with targeted panels looking at 300-600 of the most mutated genes in cancer.”

“We often see consults where physicians send specimens because the tumor looks very atypical. There may be loss of p16 expression and PRAME positivity, so it looks quite worrisome for a melanoma,” said Dr. North. “But in a 10-year-old child, you don’t want to make a melanoma diagnosis without having a full assessment of the tumor. We would get NGS on this, and sometimes it ends up being on the benign side even with the concerning features noticed in the initial workup.”

Sometimes more than one test is indicated, Dr. Gerami said. “NGS may be performed to identify the primary driver and some progression events. If the pathologist does not find anything and is still worried, then CGH or FISH may be added to look for other potential progression events.”

Next steps

With severely atypical Spitz tumors, dermatologists often want to know whether they should do a sentinel lymph node biopsy, Dr. Bridges said. “There’s no reason to do a sentinel lymph node biopsy because it has no prognostic benefit. Yes, they can have a positive sentinel lymph node biopsy, but it doesn’t predict a poor outcome in these patients, particularly pediatric patients.”

Everybody wants to know about margins, said Dr. Bridges. “If it’s anything that is atypical or severely atypical, then you have to excise it with 5-millimeter margins; you treat Spitz melanomas like any other melanoma.”

If a dermatologist receives a report in which NGS is done, if anything is not clear, call the dermatopathologist, advised Dr. North. “It’s not the same as a lab test in which there is a clear positive or negative result.” 

“It’s very easy to get confused when seeing all the next generation sequencing data. It can even confuse the molecular pathologists sometimes because there may be mutations listed in the reports that are not significant,” he continued.

“If you feel like there’s a disconnect between your clinical impression and the report, you should call the dermatopathologist to walk through everything and ask questions about whether the mutations are significant,” said Dr. North. “Don’t feel you like you have to have a grasp of everything molecular to make the call.”

“Perhaps there was not a definitive diagnosis in a biopsy without comprehensive testing,” continued Dr. North. “The call could simply be, ‘Could we do some additional testing to see if we could get a more definitive diagnosis?’ or ‘Could we get a second opinion consult with possible additional testing?’”

Dr. Gerami urges dermatologists to forge a good working relationship with their dermatopathologist and discuss cases that are concerning. “If the diagnosis is straightforward from the pathologist, then some of these molecular tests may not be needed. If they are needed, then it may be worthwhile to discuss the details of the case with the pathologist to understand the testing and what level of certainty the pathologist has of a benign or malignant diagnosis.”

Spitz pathology reports can be anxiety-inducing because of how atypical and yet how clinically unaggressive they can be, Dr. North said. “The goal should be proper treatment, not overtreatment, in these tumors that generally have a very excellent prognosis, even in that intermediate category of an atypical Spitz tumor.” 

https://www.intramed.net/content/como-leer-y-comprender-un-articulo-cientifico

¿Cómo leer y comprender un artículo científico?

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Uno de los principales pilares de la práctica médica es la investigación. Y para mejorar como profesionales, tenemos que saber cómo leer e interpretar una publicación científica.

Antes de comenzar con la lectura de un artículo, tenemos que conocer la variedad de evidencia científica que hay. Entonces:

¿Qué tipos de artículos existen? ¿Y cuáles son sus beneficios?

· Artículo original: investigaciones directas para evaluar conclusiones rescatadas del contacto con poblaciones estadísticamente relevantes.

· Reportes: pueden ser "reportes breves", que tienen el mismo objetivo y contenido que los artículos originales, pero redactados de forma resumida; o también pueden ser "reportes de casos", que buscan compartir eventos aislados relevantes.

· Artículos de revisión: publicaciones con la mayor evidencia científica y el menor sesgo. Aquí se incluyen las revisiones sistemáticas, los metanálisis y las guías (que funcionan como directrices).

· Revisiones narrativas: los autores redactan sobre su área de expertise, creando una mezcla entre evidencia y práctica personal.

· Artículos de opinión: redacción desde lo empírico (no siempre fundamentado).

· Cartas al editor: respuestas de otros profesionistas ante artículos publicados para contrastar sus conclusiones basándose en otros hallazgos.

Lo primero es únicamente "ver" el título y el abstract del artículo que deseamos evaluar, es decir, por el momento no vamos a profundizar en ninguno de estos apartados. Esto, para que podamos generar nuestra propia impresión del texto sin dejarnos llevar por los primeros resúmenes que los autores nos proponen. Para comenzar formalmente con la lectura a conciencia, el Dr. Oscar Arias nos recomienda iniciar con la introducción. Este apartado nos servirá para conocer y empaparnos del panorama que se conoce acerca del tema a evaluar; esta sección nos otorgará los antecedentes, la pregunta de investigación, y nos deja echar un vistazo a cómo los autores buscarán llenar el vacío en el conocimiento propuesto una vez que este trabajo se finalice.

Posteriormente, la recomendación es acudir a la sección de resultados e inclusive buscar las figuras y tablas expresadas. Aquí nos ilustrarán de forma esquemática el diseño del estudio, la cronología, los datos estadísticos y lo mas relevante: una simplificación de los hallazgos (que, en muchas ocasiones, cuando los manuscritos son de muy buena calidad, nos pueden otorgar gran parte de la información que necesitamos saber). Específicamente, en esta sección de "resultados", lo ideal es comenzar por la evaluación de las tablas y figuras y después dar lectura al texto redactado en este mismo apartado; la finalidad de seguir este método es formar un pensamiento crítico antes de leer lo que los autores busquen hacernos entender. Además, nos sirve para identificar cualquier irregularidad que se pudo haber producido durante la elaboración del trabajo.

Una vez que hayamos concluido con este apartado, continuaremos con la discusión y la conclusión. Aquí se nos presentará un breve resumen de la introducción (para darnos un "antes de este estudio"), otro resumen de los resultados (para darnos un "durante") e incluso también se contrastarán estos con diversos hallazgos en otros manuscritos de distintos autores sobre la misma materia a tratar (este contraste nos otorgará un "después de este estudio"). En este punto, es importante que mantengamos ese pensamiento crítico con el que comenzamos a leer el trabajo para evitar únicamente guiarnos por lo que los autores nos quieren hacer entender con el "después de este estudio"; el propósito de este pensamiento crítico es evitar (en caso de que suceda) quedarnos con un sesgo que se puede presentar en la conclusión de los autores.

En caso de que aún nos queden dudas o inquietudes en este punto, nos acercaremos al apartado de materiales y métodos, para evaluar cuál fue la verdadera estrategia creada por los autores para llegar a dichos resultados.

Continuaremos ahora con una evaluación personal. En otras palabras, tras la lectura en este orden, buscaremos identificar cuáles son nuestras conclusiones personales. Esto, para evaluar si el trabajo tiene la evidencia suficiente y nos sirve para responder la pregunta que en primera instancia nos hizo acercarnos a este manuscrito en específico.

Casi para terminar, acudiremos a las referencias utilizadas; principalmente, buscaremos las que contradigan el trabajo que recién evaluamos, para que, de forma personal, podamos contrastar ambos estudios y evaluar qué generó dicho cambio y, a su vez, si este cambio es válido.

Finalmente, regresaremos a los apartados del título y abstract para ponderar si los autores plasmaron de forma correcta el trabajo realizado. Llegado este punto, nos puede servir como herramienta el realizar un resumen sobre lo que entendimos de la lectura, para, como bien lo menciono, continuar con el pensamiento crítico.

Tener el conocimiento de la mejor evidencia actualizada, pero sin dejar de lado los conocimientos esenciales, los "artículos clásicos", pues gracias a estos podemos entender todo lo que hoy en día innova a la medicina.

Nos sirven para comprender, de forma contextualizada, el porqué de distintos escenarios en el área de la salud.

Ya para finalizar, el Dr. Oscar Arias nos comparte, a través de un artículo de su autoría, publicado en la revista npj Parkinson's Disease del portafolio de Nature, un ejemplo más extenso sobre cómo leer e interpretar un artículo médico.

A continuación, y aclarando lo anteriormente mencionado, una descripción gráfica y simplificada sobre cómo leer y obtener la mejor información de un artículo científico:

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Especial agradecimiento al Dr. Oscar Arias por su apoyo y colaboración en la realización de esta columna.

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Benjamin Hidalgo-Matlock
Skin Care Physicians of Costa Rica

Clinica Victoria en San Pedro: 4000-1054
Momentum Escazu: 2101-9574

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a mobile device.

Skin Microbiome Medicine for Dermatology - Dermatology Advisor

https://www.dermatologyadvisor.com/features/skin-microbiome-medicine/?utm_source=eloqua&utm_medium=email&utm_campaign=NWLTR_DER_UPDT_SS-LIC-LAS-PP-10205_SL_022426_AF-thisone&hmemail=arj%2Fdu47fH0tIG%2BOxiMnyzIZDo7e%2Fi8h&sha256email=818ca2c110aeb8c0905b76eae9c8cf13eeedcf69cfe6587b8903a4297c649084&hmsubid=&nid=2049200711&elqtrack=True

Breakthroughs in Skin Microbiome Medicine May Transform Dermatology

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Bryant Furlow

February 23, 2026

Human skin harbors complex microbial communities of bacteria, viruses, and fungi. A growing body of research shows that shifts in the species composition, diversity, and metabolic products of the skin ecosystem can open the door to invasion by harmful microbes, inflammatory responses, skin barrier dysfunction, and dermatologic disease.

"We have a complex relationship with our skin microbes, which are integral to immune homeostasis and repair, as well as mediators of local and systemic inflammation," explained Nathan Archer, PhD, assistant professor of dermatology at Johns Hopkins University School of Medicine.

The clinical implications of utilizing the skin microbiome in the treatment of dermatologic diseases could be profound.

Shifts in microbial community structure — especially reduced overall species diversity and the resulting predominance of pathogenic and pro-inflammatory species — precede the onset or worsening of symptoms in atopic dermatitis, eczema, acne, and psoriasis.^1-5 Large-scale genomic sequencing has identified previously unsuspected bacterial communities and microbial signatures that can help distinguish lesional skin from healthy skin, pointing toward new diagnostic and therapeutic targets.^1,5-7

Instead of viewing microbes solely as pathogens, we're beginning to harness them as therapeutic partners, designing interventions that restore microbial balance, modulate immunity, and promote repair.

Recent research has also demonstrated that disruptions of skin ecology, called dysbiosis, are more consistently associated with acne and other inflammatory dermatoses than the overgrowth of Cutibacterium acnes or Staphylococcus aureus. Dysbiosis contributes directly to disease flares, challenging longstanding assumptions about the etiology of dermatologic diseases.^4,8,9 Indeed, dysbiosis appears to be a hallmark mechanism in inflammatory dermatoses like eczema, rosacea, and psoriasis, driven by altered microbiome-immune system interactions.⁸

Scientists are exploring how ecological engineering of the skin microbiome might offer alternatives to current therapies like antibiotics, which eradicate both pathogens and beneficial microbes and may worsen dysbiosis and induce treatment resistance.^10,11

"Understanding their roles opens the door to entirely new therapeutic paradigms: instead of only suppressing inflammation, we can begin to restore balance between our skin and the microbial community," Dr Archer said.

For example, preclinical research suggests that applying commensal bacteria can improve the integrity of the skin barrier and reduce S aureus overgrowth in atopic dermatitis.^10,12 Researchers are also investigating prebiotics, strain-specific probiotics, live bacteriotherapies, genetically engineered bacteriophages, and targeted phage cocktails for selectively culling pathogens from skin ecosystems.^7,10,11,13    

The field of microbiome dermatology is young and not without significant challenges, including the need for better standardization of research methodologies and further expansion of research ventures.^4,5 Yet experts maintain optimism about knowledge gained thus far and that these challenges will be overcome. They anticipate a clinical paradigm shift toward precision microbiome medicine in the years ahead.

The Skin Microbiome Beyond the Skin

The skin's microbial ecosystem includes a dermal microbiome beneath the skin's surface and a distinct epidermal microbiome interfacing the external environment, shaped by infants' early encounters with microbes, explained Richard Gallo, MD, PhD, professor and chair of the department of dermatology at the University of California San Diego School of Medicine. Intriguingly, Dr Gallo and his colleagues found that these microbial communities communicate with the microbiomes of other organ systems, like the gut.^14,15

Skin wounds affect intestinal bacteria, for example.¹⁶ "Our work discovered that injury or inflammation of the skin causes release of 'danger signals' that are detected by cells in the intestine," Dr Gallo said. "These cells then respond by producing antimicrobials that inappropriately kill some of the bacteria in the gut that help maintain gut health. This is important as it provides an explanation for the frequent co-occurrence of diseases of the skin and gut, and emphasizes the need to treat the whole patient, not just a single organ."

This skin-to-gut axis is not the only connection between skin and other microbiomes, Dr Gallo was quick to point out. "Important communication occurs between skin and lung, skin and brain, and skin and the cardiovascular system," he explained. "With continued work, we see important general medical breakthroughs coming from understanding these communication networks."

Indeed, a recent study showed that S aureus skin exposure can exacerbate lung inflammation, helping to explain the atopic march from atopic dermatitis to respiratory disease.¹⁷

"Clinically, this highlights the importance of early intervention in atopic dermatitis — addressing microbial dysbiosis and interleukin (IL)-36-driven inflammation before diseases of the atopic march develop, such as asthma," said Dr Archer.

For patients with overlapping atopic dermatitis and neutrophilic asthma, that finding bolsters the case for a more integrated clinical approach to achieve better outcomes, Dr Archer added. "Rather than treating skin and airway disease in isolation, clinicians might consider shared immunological pathways as therapeutic targets or agents that modulate or restore healthy microbial balance that could, in principle, benefit both skin and lung inflammation," he said.

Biomarkers like IL-36 and neutrophil signatures might be helpful for risk assessment and early therapeutic escalation in patients with atopic dermatitis, to prevent neutrophilic asthma progression, Dr Archer added.

"Elevated systemic IL-36 and neutrophil signatures could identify patients whose atopic dermatitis may be leading towards neutrophilic asthma or T2-low asthma, which is more treatment-resistant than T2-high asthma," he explained. "In fact, circulating IL-36 has already been associated with severe asthma in patients."

With his coauthors, Dr Archer also reported that bacteria like S aureus can promote skin regeneration through IL-1β-dependent signaling pathways, with important implications for wound care.¹⁸

"This suggests that indiscriminate topical antibiotic use may disrupt beneficial microbe-host interactions that aid healing," Dr Archer explained. "Microbiome-aware wound care that balances pathogen control with preservation of beneficial microbes may improve regenerative outcomes."

Atopic dermatitis and asthma are heterogeneous conditions with immunological subtypes, Dr Archer pointed out, and better understanding of their mechanistic underpinnings will enable the development of more personalized treatment approaches.

"Understanding which cytokine and microbial pathways drive an individual's disease — whether it be IL-36–neutrophil, Th2, or S aureus — may enable personalized therapy selection and better prediction of comorbidities like asthma or food allergy," Dr Archer said. "We are moving away from a one-size-fits-all mentality and entering an era of precision dermatology. Instead of viewing microbes solely as pathogens, we're beginning to harness them as therapeutic partners, designing interventions that restore microbial balance, modulate immunity, and promote repair."

Are Skin Diseases Industrial Comorbidities?

In addition to genomics and molecular mechanism studies, insights into healthy skin microbiomes are being gleaned from cross-cultural research.

"Over the last few decades we've seen a steady rise in chronic inflammatory skin conditions, especially in Western countries and in places rapidly adopting Western lifestyles," explained study coauthor Julia Durack, PhD, Executive Director of the Holobiont Medical Research Foundation. "These diseases are much less common in traditional, non-industrialized communities. Because the skin microbiome is closely tied to skin health, we wanted to study the Yanomami, one of the last remaining hunter-gatherer groups, who rarely experience these conditions. By looking at their skin microbiome, we hoped to better understand what might be missing in modern populations and how that relates to the rise in skin disorders."

What they found was that the skin of this group who reside in the remote Amazonian rainforest share some bacterial communities with Western-nation populations, but with markedly greater species diversity (R² =.455; P =.001).¹⁹ A total of 115 previously unknown bacterial genomes were identified as part of the skin microbiome of these individuals.

"The Yanomami community we worked with has had very limited contact with outsiders, so it's unlikely that the shared taxa we observed were introduced by westerners. Instead, these are what we would call conserved microbial groups — taxa that are commonly found across humans and even other mammals," Dr Durack said. "What was particularly interesting in our data was that while the Yanomami share some of these same microbial groups with Western populations, the diversity within those groups was much greater. For example, their skin harbored a wider range of Staphylococcus species, including ones we didn't detect at all on Western skin. That suggests their microbiomes are not only intact but also more complex, reflecting a deeper ecological richness rather than acquisition from outside contact."

That wasn't just a reflection of the Yanomami people living in the species-rich tropics, where there are more bacterial and fungal species in general, Dr Durack said.

"People living traditional lifestyles tend to have more species-diverse skin microbiomes, and this is consistent across non-industrialized groups worldwide, not only those in the tropics," she explained. "The key factor appears to be lifestyle rather than geography. In industrialized societies, our skin microbiomes are less diverse and compositionally distinct, shaped by constant exposure to chemicals, pollution, antibiotics, and a lack of contact with beneficial microbes from soil, plants, and other natural environments."

Dr Durack and other researchers refer to conditions like acne, rosacea, psoriasis, and atopic dermatitis as industrialized comorbidities, meaning they are strongly linked to the ecological and microbial shifts that come with modernization and not something inherent to genetics or ancestry, she said.

For example, other researchers found that when urban children in Finland have more natural play areas, their skin microbiome's species diversity grows within a few weeks, along with measurable changes in immune regulation markers.²⁰

"This suggests that reintroducing environmental microbial exposures can directly influence health," Dr Durack said. "Our study extends this idea by showing that the Yanomami's continuous exposure to diverse environmental microbes likely helps maintain a complex skin microbiome. That complexity may be protective and its loss in industrialized societies could help explain the rise in inflammatory skin conditions we now consider hallmarks of modern living. Restoring microbial diversity on the skin could be an important way to boost resilience against inflammatory conditions."

The skin microbiome of a westernized adult who temporarily lived with the Yanomami shifted to Yanomami-like microbiomes, Dr Durack said, though it was lost upon their return to an industrialized setting.¹⁹

"That tells us it's not a closed door. Our skin microbiomes can adapt," she said. "In industrialized societies, we've largely lost this co-evolved relationship with our environment. While it may not be realistic to completely rewild our skin microbiomes to an ancestral state, Western medicine could take a more ecological approach: finding ways to reintroduce or support the right kinds of microbial exposures that strengthen the skin barrier and immune balance. This could open new avenues for preventive and therapeutic strategies in dermatology."

Challenges and Furthering the Research

Not surprisingly for an emerging field of knowledge, researchers caution that mechanistic uncertainties and gaps in methodological standardization must be addressed to strengthen preclinical research, and that large, well-designed, standardized clinical studies are needed to more clearly establish causality between the microbiomes and disease.^21,22

Early work with targeted bacteriophage culling has been promising so far, but little is yet known about long-term effects on commensal species, the potential for evolved resistance to phages, or off-target effects on beneficial microbes.¹³

Nor do we yet know the best strategies for ecological engraftment (defined as sustained integration of introduced species into the skin microbiome) or how species diversity and composition might affect resistance to introduced species.⁷

Yet direct-to-consumer marketing hype has gotten well ahead of the science, Dr Gallo cautioned. "An unfortunate lack of scientific rigor has occurred that has led to false claims and unrealistic expectations," he said. "The field is working through this, but several products are still sold without good scientific evidence that they are effective."

The field has taken its first tentative steps, but has yet to find its stride. "We still need to define how specific microbes and their products shape skin and systemic immunity, and when dysbiosis becomes pathologic," Dr Archer said. "This includes microbe-neuro-immune interactions, which are only beginning to be uncovered in the skin with much to be discovered about how skin microbes may affect distal neural development."

We also don't yet understand what nutrients skin microbes use, or how exactly transitions between homeostatic and inflammatory states might cause metabolic shifts in the microbiome, he noted.

"Longitudinal, mechanistic, and multi-tissue studies will be essential to close these gaps," Dr Archer said. "We are currently investigating how pathogenic bacteria gain a foothold onto our skin and why certain pathogens are commonly prevalent among multiple inflammatory skin conditions.If we can understand the strategies by pathogens to live on our skin, we hope to prevent colonization and exacerbation of inflammatory skin disorders that involve dysbiosis."

"We're only just beginning to understand how important the skin microbiome is for our overall health," agreed Dr Durack. "Most of what we know so far is based on studies of people in industrialized societies, which gives us a very narrow view. By broadening research to include communities with diverse ethnicities, lifestyles, and environments, we can uncover much more relevant insights into what truly supports healthy skin — and how modern lifestyles may be limiting that potential."

Disclosure: Weiss Biosciences Inc. funded the Yanomami skin microbiome study and paid Dr Durack's salary. Dr Nathan Archer has received previous grant support from Pfizer and Boehringer Ingelheim and was a paid consultant for Janssen Pharmaceuticals and Alphyn Biologics. Dr Gallo had no relevant disclosures.

References:

1. Chaudhary PP, Myles IA, Zeldin J, et al. Shotgun metagenomic sequencing on skin microbiome indicates dysbiosis exists prior to the onset of atopic dermatitis. Allergy. 2024;78(10):2724-2731. doi:10.1111/all.15806
2. Kim HB, Alexander H, Um JY, et al. Skin microbiome dynamics in atopic dermatitis: understanding host-microbiome interactions. Allergy Asthma Immunol Res. 2025;17(2):165-180. doi:10.4168/aair.2025.17.2.165
3. Asees A, Sadur A, Choudhary S. The skin microbiome in rosacea: mechanisms, gut-skin interactions, and therapeutic implications. Cutis. 2025;116(1):20-23. doi:10.12788/cutis/1240
4. Niedzwiedzka A, Micallef MP, Biazzo M, Podrini C. The role of the skin microbiome in acne: challenges and therapeutic opportunities. Int J Mol Sci. 2024;25(21):11422. doi:10.3390/ijms.252111422
5. Ruuskanen MO, Vats D, Potbhare R, et al. Towards standardized and reproducible research in skin microbiomes. Environ Microbiol. 2022;24(9):3840-3860. doi:10.1111/1462-2920.15945
6. Li Chengchen, Ravikrishnan A, Wijaya I, et al. Large-scale skin metagenomics reveals extensive prevalence, coordination, and functional adaptation of skin microbiome dermotypes across body sites. bioRxiv. Published online ahead of print June 8, 2025. doi:10.1101/2025.04.24.650393
7. Oh J, Voigt AY. The human skin microbiome: from metagenomes to therapeutics. Nat Rev Microbiol. Published online August 4, 2025. doi:10.1038/s41579-025-01211-9
8. Wilkhoo HS, Islam AW, Hussain S, Kadam SR, Rao ZK, Singh B. Skin microbiome and inflammatory dermatoses: a focused review. Costmoderma. 2025;5:107. doi:10.25259/CSDM_99_2025
9. Huang C, Zhuo F, Han B, et al. The updates and implications of cutaneous microbiota in acne. Cell Biosci. 2023;13:113. doi:10.1186/s13578-023-01072-w
10. Lyu Y, Shen J, Che Y, Dai L. Skin microbiome engineering: challenges and opportunities in skin disease treatment. iMetaOmics. 2025;2:e70012. doi:10.1002/imo2.70012
11. Ito Y, Amagai M. Controlling skin microbiome as a new bacteriotherapy for inflammatory skin diseases. Inflamm Regen. 2022;42:26. doi:10.1186/s41232-022-00212-y
12. Uberoi A, Murga-Garrido SM, Bhanap P, et al. Commensal-derived tryptophan metabolites fortify the skin barrier: insights from a 50-species gnotobiotic model of human skin microbiome. Cell Chem Biol. 2025;32(1):P111-P125.E6. doi:10.1016/j.chembiol.2024.12.007
13. Natarelli N, Gahoonia N, Sivamani RK. Bacteriophages and the microbiome in dermatology: the role of the phageome and a potential therapeutic strategy. Int J Mol Sci. 2023;24(3):2695. doi:10.3390/ijms24032695
14. Nakatsuji T, Chiang H, Jiang SB, Nagarajan H, Zengler K, Gallo RL. The microbiome extends to subepidermal compartments of normal skin. Nat Commun. 2013;4:1431. doi:10.1038/ncomms2441
15. Nakatsuji T, Cheng JY, Gallo RL. Mechanisms for control of skin immune function by the microbiome. Curr Opin Immunol. 2021;72:324-330. doi:10.1016/j.coi.2021.09.001
16. Dokoshi T, Chen Y, Cavagnero KJ, et al. Dermal injury drives a skin to gut axis that disrupts the intestinal microbiome and intestinal immune homeostasis in mice. Nat Commun. 2024;15:3009. doi:10.1038/s41467-024-47072-3
17. Kline SN, Feller LE, Saito Y, et al. Epicutaneous Staphylococcus aureus initiates cross-tissue IL-36R signaling for neutrophilic lung inflammation in a model of the atopic march. Cell Reports. 2025;44(8):116054. doi:10.1016/j.celrep.2025.116054
18. Wang G, Sweren E, Liu H, et al. Bacteria induce skin regeneration via IL-1β signaling. Cell Host Microbe. 2021;29(5):777-791.e6. doi:10.1016/j.chom.2021.03.003
19. Durack J, Piceno Y, Vuong H, et al. Yanomami skin microbiome complexity challenges prevailing concepts of healthy skin. Nat Comm. 2025;16:5542. doi:10.1038/s41467-025-60131-7
20. Roslund MI, Puhakka R, Grönroos M, et al. Biodiversity intervention enhances immune regulation and health-associated commensal microbiota among daycare children. Sci Adv. 2020;6(42):eaba2578. doi:10.1126/sciadv.aba2578.
21. Metwaly A, Kriaa A, Hassani Z, et al. A consensus statement on establishing causality, therapeutic applications and the use of preclinical models in microbiome research. Nat Rev Gastroenterol Hepatol. 2025;22:343-356. doi:10.1038/s41575-025-01041-3
22. Shahid U. Microbiome-guided precision medicine: mechanistic insights, multi-omics integration, and translational horizons. J Precis Med: Health Dis. 2025;3:100018. doi:10.1016/j.premed.2025.100018

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Mitos del sol y filtros

Trending Sun Protection Myths: Addressing Misinformation in Clinical Practice

12–15 minutes

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For most, sunscreen is considered the foundation of basic skin care. Yet years of hard-won progress in embracing sun safety among the public has taken a hit from recent misinformation spreading online about sun protection practices.

A 2025 study found an abundance of TikTok videos with the hashtag #nosunscreen that support many of the growing myths about sun protection, including the belief that sunscreen use is not important or may even be harmful to one's health.¹ This misinformation is quickly gaining traction, as Nikookam and colleagues reported that the #nosunscreen hashtag had surpassed 11.7 million views on TikTok while the #AntiSunscreen hashtag had garnered more than 5.3 million views at the time of their writing. These authors also reported a surge in Google searches for anti-sunscreen content.²

Dermatologist Perspectives on Sun Protection Myths

The myriad of myths regarding this topic have increasingly made their way into the dermatologist's office, with physicians reporting a growing number of patients espousing these inaccurate views.

"We are encountering an alarming rise in myths regarding sunscreen and sun protection," said Annie Grossberg, MD, associate professor of dermatology and director of pediatric dermatology at Johns Hopkins Medicine in Baltimore, Maryland.^1-3 "Some of these include misinformation about the dangers of sunscreen and the necessity of wearing sunscreen."

[T]he benefits of sunscreen in preventing melanoma and other skin cancers far outweigh theoretical risks in studies that have shown no harm of sunscreens in humans. 

Additional myths in this realm include the notions that one can develop a solar callus for sun protection or simply use coconut oil, beef tallow, or other oils in place of sunscreens approved by the United States Food and Drug Administration (US FDA).

"The rise in misinformation is likely multifactorial, but the viral nature of social media is a major contributor," Dr Grossberg said. "Influencers with broad audiences can post anecdotes or opinions and present this as factual and in a sensationalist manner, despite a lack of supporting evidence."

"Algorithm-driven platforms reward sensational natural health narratives, and influencer anecdotes travel faster than peer-reviewed data, while distrust of chemical ingredients dovetail with broader wellness and clean-beauty marketing," added dermatologist Swati Kannan, MD, associate professor of dermatology and Mohs surgeon at the University of California San Diego.

Veena Vanchinathan MD, a dermatologist and member of the American Academy of Dermatology (AAD), says that she most often hears these misconceptions from younger patients and those active on social media platforms. "Patients may ask if natural oils are better, express concerns about chemical sunscreens, or mention tanning as a way to build protection from UV damage," she shared. "These conversations often present an opportunity for me to thoughtfully partner with my patients and share impactful education."

Dr Kannan has also experienced an increase in similar questions in her practice. "Patients increasingly ask if they can swap to coconut oil, voice fears that sunscreen causes cancer, or request guidance on beef tallow recipes circulating on TikTok," she said. "My response to all of this is that we have so much evidence to support the use of sunscreen to prevent skin cancers and melanomas, and we do not have any evidence that sunscreen is carcinogenic or that natural treatments provide enough sun protection."⁴

Dr Grossberg recalls many instances of patients and parents asking about the safety of sunscreens and seeking more natural alternatives. Some parents are genuinely afraid to use sunscreens on their children due the misinformation they have heard about on social media, she explained. 

"These are well-meaning parents who want to do the best and safest things for their children and themselves, but these scenarios reflect how deeply some of this social media-driven misinformation has permeated everyday decision making," Dr Grossberg continued. "The challenge lies in redirecting these concerns towards evidence-based solutions."

6 Common Myths and Truths About Sun Protection

Below are the most common myths that dermatologists may encounter in clinical practice, as well as the accurate, evidence-based take on each point.

"Sunscreen is only necessary at the beach, on vacation, or if it's sunny outside." 

"Sun protection is essential every day, not just on vacations, at the beach, or on the hottest days of the summer," Dr Grossberg advised.⁵ "UV exposure and damage from the sun is cumulative, begins in childhood, and happens during everyday activities."

Additionally, "Up to 80% of UV rays can penetrate clouds, and UVA penetrates glass, so daily use is recommended regardless of the weather," Dr Vanchinathan noted.⁵

"Along with sun protective clothing, sunscreen remains one of the most effective tools we have for prevention of skin cancer and skin aging," Dr Grossberg said.

Both the AAD and the American Cancer Society recommend using a broad-spectrum, water-resistant sunscreen with a minimum of SPF of 30.^6,7

"People with darker skin tones don't need sunscreen."  

"While skin cancer risk may be lower in patients with skin of color, these individuals are still at risk for photoaging, pigmentary disorders, and UV-induced skin cancers," Dr Vanchinathan explained.⁸ "Daily photoprotection helps prevent pigmentary disorders such as melasma and post-inflammatory hyperpigmentation, in addition to skin cancers."

"When we eventually diagnose melanomas in darker-skinned patients, it tends to be later-stage and more aggressive disease," Dr Kannan noted.⁸ "Although melanin provides some natural SPF, it is insufficient against cumulative UV damage, so consistent sunscreen use is still recommended for all skin types."

"Sunscreen is toxic and causes cancer." 

"Approved UV filters have never shown carcinogenicity in humans, whereas UV radiation is a proven human carcinogen," Dr Kannan emphasized.⁹

"Decades of safety data and FDA evaluation support the use of both mineral and chemical sunscreens as safe and effective when used as directed," Dr Vanchinathan added. Mineral (or inorganic) sunscreens contain filters such as zinc oxide and titanium dioxide, while chemical (or organic) sunscreens contain filters such as avobenzone and octocrylene. Unlike inorganic sunscreens, organic sunscreens are designed to absorb into the skin completely.¹⁰

Patients may express concerns about the systemic absorption of chemical filters and potential associated risks, including endocrine-disrupting effects observed in some studies.^4,11,12 Although findings on this topic have been mixed overall, experts have noted the need for further study and industry testing of these potential risks linked to chemical sunscreens.^4,12,13 

"Both chemical and mineral options are safe, and patient preferences can guide their choice of which kind they want to use," Dr Kannan said. "Mineral filters remain an alternative for patient who prefer a non-absorbing option."

Dr Grossberg reiterated that the available evidence overwhelmingly shows that UV radiation from the sun is a proven carcinogen. "UV radiation is classified by the World Health Organization as a Group 1 carcinogen — in the same category as tobacco — and it is directly implicated in the development of skin cancers in humans," she said.⁹ "In contrast, concerns about sunscreen or certain sunscreen ingredients are largely theoretical and unproven, and the benefits of sunscreen in preventing melanoma and other skin cancers far outweigh theoretical risks in studies that have shown no harm of sunscreens in humans." 

"Sunscreen blocks all vitamin D production." 

"Real-world studies show that typical sunscreen use does not cause vitamin D deficiency," Dr Kannan commented.

Findings of a cross-sectional study published in 2022 showed negative correlations between sun exposure and self-reported vitamin D deficiency among US adults. No association was found between sunscreen use and vitamin D deficiency, similar to results observed in previous studies.¹⁴

"Brief incidental sun exposure, oral vitamin D supplementation, and certain foods maintain adequate 25-OH vitamin D levels without sacrificing skin integrity," Dr Kannan explained. Food sources of vitamin D include egg yolks, fatty fish, and red meat, as well as fortified foods and beverages including cereals and milk.¹⁴

"Natural oils like coconut oil or beef tallow provide adequate sun protection."

"The idea that natural oils, such as coconut oil, offer meaningful protection from the sun's harmful UV rays is simply false," Dr Grossberg stated. "While some natural oils may have SPF ranging from 2 to 8, this is well below the protection needed to prevent skin cancer or sun damage."¹⁵

These oils also "lack UVA coverage, degrade quickly, and fail water-resistance standards," Dr Kannan added. "Relying on these oils for sun protection invites cumulative DNA damage, skin cancers, and photoaging down the road."

"Coconut oil and similar substances cannot replace FDA-approved sunscreens," Dr Vanchinathan said.

"Developing a solar callus can protect the skin from UV damage." 

"The idea that you can build up a natural resistance to UV exposure over time is another that has become popular recently," according to Dr Grossberg. "However, a solar callus — or skin hardening, as it's sometimes called — is really just another term for a getting a tan and does not meaningfully increase resistance to or provide protection from solar radiation."

"While melanin provides a minimal degree of additional protection, tanning reflects DNA damage and does not prevent further UV harm," Dr Vanchinathan said.

"A tan does not provide protection against the sun, and there is no such thing as safe tan," Dr Kannan stated. "It's better to use clothing and sunscreen for sun protection."

Dr Grossberg emphasized the need for clinicians to correct misconceptions about sun protection while acknowledging patient concerns and remaining non-judgmental. "Often, when our patients or their family members learn they may be putting themselves or their children at increased risk for skin cancer, they are open to more discussion on how to mitigate these risks," she said. "Taking the time to explain the safety data behind our sunscreen recommendations goes a long way."

To address sun protection myths in the clinic, providers should "invite questions, acknowledge concerns, then share concise data and provide take-home infographics in plain language," Dr Kannan recommended.⁹ "Partner with colleagues who specialize in primary care, pediatrics, and obstetrics and gynecology to ensure consistent messaging across specialties."

To counter sun protection myths on social media, "Clinicians engaging credible voices online and also creating their own dynamic, evidence-based social media content can help counteract misinformation," Dr Vanchinathan explained.

For dermatologists creating their own content, "Produce short, engaging reels debunking single myths (for example, beef tallow ≠ sunscreen), use trending audio for reach, and link to peer-reviewed summaries," Dr Kannan advised. She further suggested working with social platforms to "flag demonstrably false health claims and boost evidence-based content."

Public Health and Community Efforts

Along with efforts to correct sun protection myths in the clinic, ongoing public health measures and community-based approaches are needed.¹⁶

"Public health campaigns that are modernized and accessible can help counter this misinformation trend," Dr Grossberg said. "These may include leveraging social media with dermatologist-backed content, promoting sun safety in schools, as well as regulating marketing that falsely promotes some of these unsafe or less effective products." She also cited the need to encourage companies to share product safety data transparently.

Dr Kannan suggested the implementation of national UV-safety campaigns modeled on anti-tobacco efforts, featuring real melanoma survivors and clear calls to action. Additional recommendations include the integration of photoprotection education into school curricula, engagement in community outreach by offering brief sun-safety sessions at local schools and community centers, and provision of free skin cancer screenings at workplaces, beaches, and sporting events to normalize sunscreen as routine health care.

Dr Kannan also noted that sunscreen is 1 pillar of sun protection and that "UV protective clothing, wide-brimmed hats, midday shade, and behavior change can multiply protection and lessen dependence on any single modality."¹⁷  

References:

 

1. Herman C, Harb N, Ghazarian M, Belzile E, Morena N, Meguerditchian AN. BIO25-022: why don't they want to wear sunscreen? quantifying anti-sunscreen messaging on TikTok. J Natl Compr Canc Netw. 2025;23(3.5):BIO25-022. doi:10.6004/jnccn.2024.7105
2. Nikookam Y, Potluru A, Guckian J. Comment on 'a cross-sectional analysis of TikTok content relating to sunscreen conspiracy theories and correlation with published evidence on sunscreen risks': debunking sunscreen myths and trends – lessons for dermatology educators. Clin Exp Dermatol. 2025;50(5):1025–1027. doi:10.1093/ced/llae492
3. Silva HM. Misinformation about sunscreens on Brazilian social networks: a risk to public health. Trends in Medical Research. 2024;19(1):285-292. doi.org:10.3923/tmr.2024.285.292
4. Sander M, Sander M, Burbidge T, Beecker J. The efficacy and safety of sunscreen use for the prevention of skin cancer. CMAJ. 2020;192(50):E1802-E1808. doi:10.1503/cmaj.201085
5. Dale Wilson B, Moon S, Armstrong F. Comprehensive review of ultraviolet radiation and the current status on sunscreens. J Clin Aesthet Dermatol. 2012;5(9):18-23. Accessed August 9, 2025. https://pmc.ncbi.nlm.nih.gov/articles/PMC3460660/pdf/jcad_5_9_18.pdf
6. American Academy of Dermatology. What to wear to protect your skin from the sun. Accessed August 9, 2025. https://www.aad.org/public/everyday-care/sun-protection/shade-clothing-sunscreen/what-to-wear-protect-skin-from-sun
7. American Cancer Society. Spend time outside and stay sun-safe. Published March 7, 2025. Accessed August 9, 2025. https://www.cancer.org/cancer/latest-news/stay-sun-safe-this-summer.html
8. Brar G, Dhaliwal A, Brar AS, et al. A comprehensive review of the role of UV radiation in photoaging processes between different types of skin. Cureus. 2025;17(3):e81109. doi:10.7759/cureus.81109
9. The World Medical Association. WMA statement on solar radiation and photoprotection. Published October 26, 2021. Accessed August 9, 2025. https://www.wma.net/policies-post/wma-statement-on-solar-radiation-and-photoprotection/
10. Raymond-Lezman JR, Riskin SI. Sunscreen safety and efficacy for the prevention of cutaneous neoplasm. Cureus. 2024;16(3):e56369. doi:10.7759/cureus.56369
11. Matta MK, Florian J, Zusterzeel R, et al. Effect of sunscreen application on plasma concentration of sunscreen active ingredients: a randomized clinical trial. JAMA. 2020;323(3):256-267. doi:10.1001/jama.2019.20747
12. Jaskulak M, Cinkusz M, Franchuk K, Zorena K. Endocrine and reproductive health considerations of sunscreen UV filters: insights from a comprehensive review 2014-2024. Curr Environ Health Rep. 2025;12(1):28. doi:10.1007/s40572-025-00492-9
13. US Food and Drug Administration. FDA In Brief: FDA announces results from second sunscreen absorption study. Published January 20, 2020. Accessed August 9, 2025. https://www.wma.net/policies-post/wma-statement-on-solar-radiation-and-photoprotection/
14. Andrade JM, Grandoff PG, Schneider ST. Vitamin D intake and factors associated with self-reported vitamin D deficiency among US adults: a 2021 cross-sectional study. Front Nutr. 2022;9:899300. doi:10.3389/fnut.2022.899300
15. Arkhipenko Z, Shah SC, Yi RC, Feldman SR. A review on homemade sunscreen. Journal of Integrative Dermatology. Published online April 7, 2025. Accessed August 9, 2025.
16. Love B, Ghosh C, Oestman K, et al. Understanding the impact of community-based sun safety interventions on a college campus in Texas. J Am Coll Health. 2024:1-8. doi:10.1080/07448481.2024.2367989
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Tori Rodriguez, MA, LPC, AHC

FDA Alert Highlights DPD Deficiency Warnings for 5-FU, Capecitabine - Dermatology Advisor

https://www.dermatologyadvisor.com/news/fda-alert-highlights-dpd-deficiency-warnings-for-5-fu-capecitabine/?utm_source=eloqua&utm_medium=email&utm_campaign=NWLTR_DER_UPDT_SS-LIC-LAS-PP-10041_SL_021126_AF&hmemail=arj%2Fdu47fH0tIG%2BOxiMnyzIZDo7e%2Fi8h&sha256email=818ca2c110aeb8c0905b76eae9c8cf13eeedcf69cfe6587b8903a4297c649084&hmsubid=&nid=2049200711&elqtrack=True

FDA Alert Highlights DPD Deficiency Warnings for 5-FU, Capecitabine

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February 10, 2026

The Food and Drug Administration (FDA) has issued a safety alert to increase awareness of previous updates to the prescribing label for capecitabine (Xeloda^®) and fluorouracil (5-FU) products related to risks associated with dihydropyrimidine dehydrogenase (DPD) deficiency.

Capecitabine and 5-FU are both nucleoside metabolic inhibitors approved for various cancers. Capecitabine is indicated for colorectal, breast, gastric, esophageal, gastroesophageal junction, and pancreatic cancers, while 5-FU is indicated intravenously for adenocarcinomas of the colon, rectum, breast, stomach, and pancreas, as well as topically for multiple actinic or solar keratoses and superficial basal cell carcinoma. 

According to the safety alert, patients with specific homozygous or compound heterozygous variants in the DYPD gene are at a greater risk for toxicity. These variants lead to a deficiency of the DPD enzyme, which is responsible for breaking down more than 80% of 5-FU. As a result, exposure to capecitabine or 5-FU in these patients can lead to acute early-onset toxicity as well as other serious adverse reactions, such as mucositis, diarrhea, neutropenia, and neurotoxicity.

In response, the FDA approved various safety revisions to the capecitabine and 5-FU product labels. Specifically, a new boxed warning was added to note the risk of serious adverse reactions or death in patients with complete DPD deficiency. The warning further advises that DPYD testing be performed prior to starting capecitabine or 5-FU, unless immediate treatment is necessary. If testing shows complete DPD deficiency, treatment with these nucleoside metabolic inhibitor therapies should be avoided entirely.

The prescribing information was also updated to include a new subsection in the Dosage and Administration and Warnings and Precautions sections to reiterate the need for evaluation and testing for DPD deficiency before starting capecitabine or 5-FU. Moreover, the new labeling highlights the need for caution in those with partial DPD deficiency, emphasizing that dosages for these patients should be individualized and modified based on tolerability and intent of treatment.

The FDA recommends that all health care providers be aware of the risks of DPD deficiency and test for DPYD genetic variants prior to starting treatment, except in cases where immediate treatment is necessary. Additionally, providers should inform patients prior to treatment with capecitabine or 5-FU of the potential toxicities associated with DPD deficiency. 

Adverse reactions associated with the use of capecitabine or 5-FU should be reported to the FDA's MedWatch program.

This article originally appeared on MPR

US Food and Drug Administration. Safety labeling update for capecitabine and fluorouracil (5-FU) on risks associated with dihydropyrimidine dehydrogenase (DPD) deficiency. February 5, 2026. https://www.fda.gov/drugs/resources-information-approved-drugs/safety-labeling-update-capecitabine-and-fluorouracil-5-fu-risks-associated-dihydropyrimidine. 

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Benjamin Hidalgo-Matlock
Skin Care Physicians of Costa Rica

Clinica Victoria en San Pedro: 4000-1054
Momentum Escazu: 2101-9574

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